Plasmid prophage P1 is one of the simplest genomes that enjoys segregational stability as a consequence of (a) controlled replication, (b) a partition mechanism, and (c) a fail-safe mechanism that can kill cells from which this non-essential genome has been lost. (a). The effective binding of the replication initiator protein RepA of plasmid P1 to the origin it activates is controlled by chaperones. They can play a role in vitro of converting the inert dimeric form of RepA into active monomers. Physical measurements previously suggested that in vivo chaperones assist monomerization indirectly by mediating a conformational change in a predominantly monomeric form of RepA. Support for this view comes from studies of mutants defective in RepA dimerization that are found to retain chaperone-dependence for DNA binding. We are also interested in the role of RepA in strand-opening. In vivo studies indicate that the role of RepA is to assist strand-opening (as detected by reactivity of the DNA with permanganate) by the host initiator DnaA. (b) P1 contributes two proteins, ParA and ParB, and a centromere analog, parS, to a partition apparatus. A novel selection for partition-defective mutants that exploits a dysfunctional interaction between ParB and parS was previously developed. A characterization of ParB mutants thus obtained indicates that a C-terminal region of the protein is required for dimerization and binding to parS. Evidence that a +1 ribosomal frameshift in a particular mutant can partially compensate for a -1 frameshift in a particular mutant resolves an apparent inconsistency in the analysis. The dysfunctional ParB-parS interaction mentioned above may possibly involve a polymerization of ParB along the DNA from a nucleation site in parS such that the covered DNA is silenced. Conditions for testing this hypothesis are being developed. (c) P1 encodes an endotoxin (Doc) that can cause death on curing a host of its plasmid and an antidote (Phd) that prevents host death during plasmid maintenance. The relative instability of the antidote means that the cessation of transcription of the phd-doc operon can be lethal. Fluctuations in transcription of the operon are damped by an autoregulatory circuit in which both Phd and Doc participate. Mutants in phd and doc that affect specific separable functions have been isolated.